Molecular mechanisms of pain in the anterior cingulate cortex

Publisher Website
Google Scholar
Abstract
It is well known that peripheral sensory stimuli, including pain, trigger a series of neuronal activities along the somatosensory pathways as well as the neuronal network in the high brain structures. These neuronal activities not only produce appropriate physiological responses but also induce long‐term plastic changes in some of the central synapses. It is believed that long‐term synaptic changes help the brain to process and store new information. Such learning is critical for animals and humans to gain new knowledge of changing enviornment, generate appropriate emotional responses, and avoid dangerous stimuli in the future. In the case of permanent injury, however, the brain fails to distinguish the difference between “useful” and painful stimuli. Long‐term synaptic changes work against the system and at least in part contribute to chronic pain. In this short article, the possible molecular mechanisms for long‐term plasticity within the anterior cingulate cortex (ACC) will be discussed and reviewed, and it is hypothesized that potentiation of excitatory responses within the ACC contributes to chronic pain and pain‐related mental disorders.